The DOI matches its Crossref record; 90 of the 90 references it cites were found in a registry or an index.
UPR, autophagy, and mitochondria crosstalk underlies the ER stress response
Open accessAbstract
Cellular stress, induced by external or internal cues, activates several well-orchestrated processes aimed at either restoring cellular homeostasis or committing to cell death. Those processes include the unfolded protein response (UPR), autophagy, hypoxia, and mitochondrial function, which are part of the global endoplasmic reticulum (ER) stress (ERS) response. When one of the ERS elements is impaired, as often occurs under pathological conditions, overall cellular homeostasis may be perturbed. Further, activation of the UPR could trigger changes in mitochondrial function or autophagy, which could modulate the UPR, exemplifying crosstalk processes. Among the numerous factors that control the magnitude or duration of these processes are ubiquitin ligases, which govern overall cellular stress outcomes. Here we summarize crosstalk among the fundamental processes governing ERS responses.
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“To mitigate or manage ER stress, C. albicans cells utilize the UPR pathway, which plays a crucial role in restoring homeostasis and normal ER function [41].”
From Disruption of the UPC2 Gene Enhances Fluconazole Antifungal Activity by Inhibiting HAC1 mRNA Splicing in Candida albicans (2026) · cites this paper as [41]
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“Disruptions in ER homeostasis, such as the accumulation of misfolded proteins or disturbances in Ca2+ signaling, activate the UPR pathway, an adaptive signaling pathway aimed at restoring proteostasis [41].”
From Disruption of the UPC2 Gene Enhances Fluconazole Antifungal Activity by Inhibiting HAC1 mRNA Splicing in Candida albicans (2026) · cites this paper as [41]
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Cites
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Jiang, Y., Wang, Z., Ma, B., Fan, L., Yi, N., Lu, B., Wang, Q., & Liu, R. (2018) · Frontiers in Pharmacology · doi:10.3389/fphar.2018.01168 · Cited by 88
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Nie, Z., Chen, M., Wen, X., Gao, Y., Huang, D., Cao, H., Peng, Y., Guo, N., Ni, J., & Zhang, S. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.683940 · Cited by 43
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The activation of autophagy protects neurons and astrocytes against bilirubin-induced cytotoxicity
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“Disruptions in ER homeostasis, such as the accumulation of misfolded proteins or disturbances in Ca 2+ signaling, activate the UPR pathway, an adaptive signaling pathway aimed at restoring proteostasis [41].”
Metadata
- Authors
- Senft, D., & Ronai, Z. A.
- Affiliations
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Senft, Daniela
- Ronai, Ze’ev A.
- Venue
- Trends in Biochemical Sciences
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 40
- Issue
- 3
- Pages
- 141-148
- ISSN
- 0968-0004 (ISSN-L)
- PMC
- PMC4340752
- OpenAlex
- W2019263782
- Cited by
- 1,121
- References
- 90
- Citations by year
- 2026: 84 · 2025: 116 · 2024: 113 · 2023: 148 · 2022: 130 · 2021: 107 · 2020: 105 · 2019: 95 · 2018: 72 · 2017: 70 · 2016: 61 · 2015: 20
- FWCI
- 7.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Trends in Biochemical Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (P01CA128814, CA-128814, P30CA030199)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- unfolded protein response, autophagy, mitochondrial function, endoplasmic reticulum stress, ubiquitin ligase, cellular stress response, cell death, cellular homeostasis
- MeSH terms
- Animals, Autophagy, Cell Physiological Phenomena, Humans, Mitochondria, Stress, Physiological, Unfolded Protein Response, Endoplasmic Reticulum Stress
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